Herpetic imprint on privileged areas of its target organs: local latency and reactivation in herpetic keratitis.

Herpetic ocular disease is still one of the major causes of corneal blindness. Due to its unique morphological structure, the eye is one of the most studied organs--in both clinical and experimental models of herpetic infections. Herpes simplex virus (HSV) can react with human host cells to produce cytocidal infection, persistent infection, or latent infection. Whilst the establishment of viral latency in the sensory ganglia was demonstrated and extensively studied, recent evidences based on: (a) demonstration of viral particles by electron microscopy and of HSV positive antigen cells in human corneae with inactive stromal keratitis; (b) experimental animal and in vitro studies with the use of organ cultures, co-cultivation methods and molecular biology techniques; suggest the possibility of local latency in non-neural tissues as an additional source of dormant viruses that could reactivate and lead to local reinfection of the affected target organ. Reactivation of a herpetic infection may therefore require both the existence of a dormant herpetic reservoir in the ganglia, and a predilected target organ with possible independent mechanisms of local latency and reactivation. Possible mechanisms of triggers for reactivation of herpetic ocular disease are discussed.